Mechanism of Hematuria

Abstract

A model of hematuria was established in rabbits. An accelerated form of unilateral Masugi nephritis was induced in 10 New Zealand white rabbits by an intravenous injection of duck antirabbit kidney serum and by ligating the left renal artery immediately after the injection of the antibody. All 10 rabbits became hematuric 1–2 weeks after the injection of the antibody and red blood cell (RBC) casts were found in the urinary sediment of all these animals. An ultrastructural examination of renal glomeruli by transmission electron microscopy revealed the transcapillary passage of polymorphonuclear leukocytes through the gaps of the glomerular basement membrane (GBM). RBC were found in the urinary space in 50% of the glomeruli observed by scanning electron microscopy (SEM) and the passage of leukocytes and RBCs through the glomerular capillary wall was also observed. Gaps in the GBM became clearer after the removal of cellular components by detergents. In control rabbits, no RBCs could be observed in the urinary space, and isolated GBM were intact by SEM. These data further support the hypothesis that in rabbit Masugi nephritis hematuria is a result of the passage of RBCs through gaps in the GBM.

Escape of Red Blood Cells through Gaps in Glomerular Basement Membrane in a Patient with Mixed Connective Tissue Disease

“…In the same man ner, we previously demonstrated linear defects in the basement membrane [11,12]. H o w e v e r, in the present case, we failed to observe gaps in the GBM by this proce dure.…”

“…Bohle et al [6] demonstrated the escape of RBCs by scanning elec tron microscopy as well as by regular transmission elec tron microscopy in patients with mild mesangioproliferative glomerulonephritis. We also demonstrated the escape of RBCs from the rupture of the glomerular capillary wall by both transmission and scanning electron microscopy in animal models of hematuria [11,12], One characteristic of glomerular bleeding is the finding of dysmorphic RBCs in the urine. Several investigators [13,14] suggest that RBCs that originate in the glomeru lus are dysmorphic, whereas those that originate in other parts of the urinary tract are uniformly isomorphic.…”

Dynamic Analysis on Rupture of Glomerular Basement Membranes in Glomerulonephritis

“…We previously reported in Nephron that the hematuria observed in patients with glomerulonephritis was caused by a rupture of the glomerular basement membrane [1], a layer that had the strongest resistance to stretching among three layers within the cylindrical capillary wall, and had a three-dimensional meshwork structure composed of fine pores and fibrils and having an isotropic property [2, 3]. Using scanning electron microscopy, we noticed that the split lines caused by the ruptures of the glomerular basement membranes were almost always linear in shape and that they were frequently parallel to the axis of the capillary.…”